For ethical and economic reasons, when patients are acutely ill with catatonia and melancholia, ECT is best considered sooner rather than later.
Charles H. Kellner, MD
Simply telling patients “we don’t know how ECT works” neglects our abundant knowledge of what this treatment does. The authors review biological actions of ECT and discuss future directions for research.
This review covers recent advances in ECT technique, post-ECT management, and theories of mechanism of action. It will focus on the use of ECT in depression, the most common indication for ECT in clinical practice.
Some recent breakthroughs, using newly developed neuroscience investigational tools, suggest that if research resources are available, we could soon make substantial advances in understanding the mechanism of action of ECT.
The authors review the clinical use of ketamine as the anesthetic induction agent in ECT and discuss the evidence that it augments antidepressant response and reduces cognitive adverse effects.
Catatonia—a syndrome of disturbed motor, mood, and systemic signs (eg, rigidity, immobility, mutism, staring, posturing, waxy flexibility, echopraxia, echolalia, and stereotypies)—has led to the clarification of its appropriate treatment.
For patients with treatment-resistant depression—especially geriatric patients—ECT is a viable treatment option . . . one that should no longer be relegated to the option of last resort.
Here we discuss how advancements in anesthesia techniques and ECT procedures make ECT more comfortable and tolerable for patients.
Simple, standardized protocols ensure that ECT can be provided safely and comfortably in many facilities, with consistent anti-depressant results and a favorable adverse-effect profile.
A balanced review of the safety and efficacy of ECT is needed, which does not mean weighing anecdotal reports of memory loss equally with systematically collected clinical data.